inflammation surely ths wl help u all

1. DR. Murali B MDR. Murali B M
INFLAMMATIONINFLAMMATION

2. INFLAMMATIONINFLAMMATION
DEFINITION
INFLAMMATION IS A HOST RESPONSEINFLAMMATION IS A HOST RESPONSE
TO LOCAL INJURYTO LOCAL INJURY
IT IS FUNDAMENTALLY A VASCULARIT IS FUNDAMENTALLY A VASCULAR
PHENOMENON.PHENOMENON.
The suffix “itis” is added to the base word toThe suffix “itis” is added to the base word to
state the condition in inflammation. E.g.state the condition in inflammation. E.g.
Appendix -appendicitis & Gingiva -gingivitisAppendix -appendicitis & Gingiva -gingivitis

3. INFLAMMATION-HISTORICALINFLAMMATION-HISTORICAL
ASPECTSASPECTS
4 ANCIENT CARDINAL SIGNS –DESCRIBED BY CELSUS IN 14 ANCIENT CARDINAL SIGNS –DESCRIBED BY CELSUS IN 1STST
CENTURY A.DCENTURY A.D
 RUBOR-RUBOR-REDNESSREDNESS
 CALOR-CALOR-HEATHEAT
 TUMOR-TUMOR-SWELLINGSWELLING
 DOLOR-DOLOR-PAINPAIN
55THTH
SIGN DESCRIBED BY RUDOLF VIRCHOWSIGN DESCRIBED BY RUDOLF VIRCHOW
 LOSS OF FUNCTIONLOSS OF FUNCTION (FUNCTIO LAESA) -(FUNCTIO LAESA) -

4. CARDINAL SIGNS OFCARDINAL SIGNS OF
INFLAMMATIONINFLAMMATION


5. INFLAMMATION-STIMULIINFLAMMATION-STIMULI
 PHYSICAL AGENTSPHYSICAL AGENTS-Trauma, Thermal-Trauma, Thermal
injury &Radiation injuryinjury &Radiation injury
 CHEMICAL AGENTS-CHEMICAL AGENTS- Acids, Alkalis,Acids, Alkalis,
Toxins & PoisonsToxins & Poisons
 BIOLOGICAL AGENTSBIOLOGICAL AGENTS – Infections:– Infections:
Bacterial, Viral, Fungal & ParasiticBacterial, Viral, Fungal & Parasitic
 TISSUE NECROSISTISSUE NECROSIS
 FOREIGN BODYFOREIGN BODY
 IMMUNOLOGICAL INJURIESIMMUNOLOGICAL INJURIES

6. Cells of inflammationCells of inflammation
CellCell ActivityActivity PhagocytosisPhagocytosis InflammationInflammation
NeutrophilNeutrophil Proteases,Proteases,
oxidasesoxidases
++ AcuteAcute
EosinophilEosinophil AntihistamineAntihistamine ++ Acute, chronicAcute, chronic
MacrophageMacrophage
(modified(modified
monocytes)monocytes)
AntigenAntigen
processing,processing,
digestiondigestion
++ Late acute,Late acute,
chronicchronic
LymphocyteLymphocyte LymphokinesLymphokines -- ChronicChronic
Plasma cellPlasma cell AntibodyAntibody
productionproduction
-- ChronicChronic

7. Cells of the inflammatory processCells of the inflammatory process
 NeutrophilsNeutrophils. These are the first inflammatory cells on the scene after. These are the first inflammatory cells on the scene after
tissue injury. They phagocytize a foreign material (e.g. bacteria) and thentissue injury. They phagocytize a foreign material (e.g. bacteria) and then
attempt to oxidize and digest it through oxidase and proteasesattempt to oxidize and digest it through oxidase and proteases
 EosinophilsEosinophils are also phagocytic and possess many of the enzymes of theare also phagocytic and possess many of the enzymes of the
neutrophil. In addition, they can dispense antihistamine in an area ofneutrophil. In addition, they can dispense antihistamine in an area of
histamine release. Thehistamine release. The eosinophileosinophil is also associated with allergicis also associated with allergic
responses. It is seen in both acute and chronic inflammation and becomeresponses. It is seen in both acute and chronic inflammation and become
increased in parasitic infestationsincreased in parasitic infestations
 MacrophagesMacrophages: Monocytes and tissue macrophages. They engulf the: Monocytes and tissue macrophages. They engulf the
foreign particles at the site of entry and process their antigens and feedsforeign particles at the site of entry and process their antigens and feeds
this information immune system to mount immune response throughthis information immune system to mount immune response through
humoural (antibody) and cell mediated immune mechanismshumoural (antibody) and cell mediated immune mechanisms
 LymphocytesLymphocytes are simple-appearing cells with varied and complexare simple-appearing cells with varied and complex
functions. The lymphocytes are classifed into T-lymphocytes and B-functions. The lymphocytes are classifed into T-lymphocytes and B-
lymphocytes. T-lymphoctyes function mediate cellular immune responselymphocytes. T-lymphoctyes function mediate cellular immune response
through production various type of lymphokines, which have local effects onthrough production various type of lymphokines, which have local effects on
other cells. B- lymphocytes medicate antibody respones throughother cells. B- lymphocytes medicate antibody respones through
production of Immunoglobulins or antibodies. The lymphocytesproduction of Immunoglobulins or antibodies. The lymphocytes
characterizes chronic inflammation. Antibody production is the function ofcharacterizes chronic inflammation. Antibody production is the function of
the plasma cellthe plasma cell, a specialized B cell, which is also found in chronic, a specialized B cell, which is also found in chronic
inflammation. It is especially prominent in chronic inflammation involvinginflammation. It is especially prominent in chronic inflammation involving
mucosal surfacesmucosal surfaces

8. INFLAMMATION-TYPESINFLAMMATION-TYPES
ACUTEACUTE
 RAPID ONSETRAPID ONSET
 SHORT DURATIONSHORT DURATION
 EXUDATION OF FLUID AND PLASMA PROTEINSEXUDATION OF FLUID AND PLASMA PROTEINS
 NEUTROPHIL IS THE PREDOMINANT WBCNEUTROPHIL IS THE PREDOMINANT WBC
 StereotypicStereotypic
 CHRONICCHRONIC
 SLOW ONSETSLOW ONSET
 LONGER DURATIONLONGER DURATION
 LYMPHOCYTES AND MACROPHAGESLYMPHOCYTES AND MACROPHAGES
 PROLIFERATION OF BLOOD VESSELS AND FIBROSISPROLIFERATION OF BLOOD VESSELS AND FIBROSIS
 Granulomatous inflammation is also regarded asGranulomatous inflammation is also regarded as
a type of chronic inflammationa type of chronic inflammation

9. ACUTE INFLAMMATIONACUTE INFLAMMATION
 Systemic responseSystemic response of Acute inflammationof Acute inflammation::
Systemically, acute inflammation may beSystemically, acute inflammation may be
accompanied by fever. There may be aaccompanied by fever. There may be a
peripheral blood leukocytosis, especially ofperipheral blood leukocytosis, especially of
neutrophils, along with increased number ofneutrophils, along with increased number of
immature forms of neutrophils (“left shift”).immature forms of neutrophils (“left shift”).
Presence of Acute phase reactants in blood eg.Presence of Acute phase reactants in blood eg.
C-reactive protein.C-reactive protein.
 Local responseLocal response of Acute inflammationof Acute inflammation::
includeinclude
 VASCULAR CHANGESVASCULAR CHANGES
 CELLULAR EVENTSCELLULAR EVENTS

10. Vascular changes in Acute inflammationVascular changes in Acute inflammation
Locally, it isLocally, it is the vascular responsethe vascular response to tissue injury that isto tissue injury that is
fundamental. The changes are seen in arterioles, capillariesfundamental. The changes are seen in arterioles, capillaries
and venules.and venules.
 The initial response to tissue injury is an episode lastingThe initial response to tissue injury is an episode lasting
from seconds to 5 minutes.from seconds to 5 minutes.
 TransientTransient vasoconstrictionvasoconstriction, probably as a direct effect on, probably as a direct effect on
the vessels.the vessels.
 Followed byFollowed by VasodilatationVasodilatation of the precapillary arteriolesof the precapillary arterioles
resulting in greater blood flow to the area. This lasts as longresulting in greater blood flow to the area. This lasts as long
as the acute inflammation persists. The injured areaas the acute inflammation persists. The injured area
reddens fromreddens from increased blood flowincreased blood flow;;
 this is accompanied bythis is accompanied by increased vascular permeabilityincreased vascular permeability..
As a consequence,As a consequence, interstitial edemainterstitial edema (swelling) occurs(swelling) occurs
owing to the escape of intravascular fluid, called an exudate.owing to the escape of intravascular fluid, called an exudate.
This is important to bring Antibodies and leukocytes to siteThis is important to bring Antibodies and leukocytes to site
of injury.of injury.
 Then, the lymphatic vessels admit the escaped fluid intoThen, the lymphatic vessels admit the escaped fluid into
the lymphatic system and after several days the swellingthe lymphatic system and after several days the swelling
subsides.subsides.

11. Transudate, exudate and pus..
AA transudatetransudate results when increased intravascular fluidresults when increased intravascular fluid
escapes into the interstitial tissues due toescapes into the interstitial tissues due to increasedincreased
hydrostatic pressurehydrostatic pressure in the vessels. Vascular permeability isin the vessels. Vascular permeability is
intact. A good example is the pedal (ankle) edema seen inintact. A good example is the pedal (ankle) edema seen in
congestive heart failure. This fluid has low protein contentcongestive heart failure. This fluid has low protein content
and specific gravity (< 1.020).The cells present are fewand specific gravity (< 1.020).The cells present are few
lymphocytes.lymphocytes.
In acute inflammation, the edema is caused by the escape ofIn acute inflammation, the edema is caused by the escape of
fluid into the interstitial tissues due tofluid into the interstitial tissues due to increased vascularincreased vascular
permeability of endothelial cellspermeability of endothelial cells. This fluid is called an. This fluid is called an
exudateexudate. Because more protein escapes with the fluid. Because more protein escapes with the fluid
compared with that which occurs with a transudate, ancompared with that which occurs with a transudate, an
exudate has a higher protein content and specific gravity (>exudate has a higher protein content and specific gravity (>
1.020). More inflammatory cells (Neutrophils & Macrophages)1.020). More inflammatory cells (Neutrophils & Macrophages)
PusPus consists mostly of neutrophils and necrotic derbis, beingconsists mostly of neutrophils and necrotic derbis, being
high in protein content with a specific gravity greater thanhigh in protein content with a specific gravity greater than
1.020.1.020.

12. Characteristics of transudate, exudate and pusCharacteristics of transudate, exudate and pus
Fluid typeFluid type ConditionCondition ContentContent SpecificSpecific
gravitygravity
TransudateTransudate Increase hydrostaticIncrease hydrostatic
pressure (CCF,pressure (CCF,
Cirrhosis liver)Cirrhosis liver)
Low proteinLow protein < 1.020< 1.020
ExudateExudate Acute inflammationAcute inflammation High proteinHigh protein > 1.020> 1.020
PusPus Acute inflammationAcute inflammation High proteinHigh protein
plus neutrophilsplus neutrophils
> 1.020> 1.020

13. Cellular Events of InflammationCellular Events of Inflammation
MarginationMargination
Adhesion & rollingAdhesion & rolling
PavementationPavementation
Emigration &Emigration &
DiapedesisDiapedesis
ChemotaxisChemotaxis
PhagocytosisPhagocytosis

14. Cellular eventsCellular events in acute inflammationin acute inflammation..
 Cellular events begin soon after vasodilatation. LeukocytesCellular events begin soon after vasodilatation. Leukocytes
(especially polymorphonuclear leukocytes) move from the center of(especially polymorphonuclear leukocytes) move from the center of
the blood column in a vessel to the peripherythe blood column in a vessel to the periphery (margination)(margination) andand
they startthey start rolling (tumbling)rolling (tumbling) on the endothelial surface. Later beginon the endothelial surface. Later begin
to adhereto adhere (adhesion)(adhesion) to the endothelial surface with the help ofto the endothelial surface with the help of
adhesion molecules (Selectins and integrins) resulting in coveringadhesion molecules (Selectins and integrins) resulting in covering
of endothelial surfaceof endothelial surface (pavementing).(pavementing).
 At the same time, the leukocytes move from the vessels into theAt the same time, the leukocytes move from the vessels into the
interstitial tissuesinterstitial tissues (emigration)(emigration) by forcing through endothelialby forcing through endothelial
junctionsjunctions..
 Once outside the vessel they start moving towards site of injuryOnce outside the vessel they start moving towards site of injury
with the help of chemical mediatorswith the help of chemical mediators (Chemotaxis).(Chemotaxis).
 Once they reach the site of injury the neutrophils engulf theOnce they reach the site of injury the neutrophils engulf the
injurious agentinjurious agent (Phagocytosis)(Phagocytosis) and tries to destroy them usingand tries to destroy them using
their proteolytic enzymes & oxygen derived free radicalstheir proteolytic enzymes & oxygen derived free radicals
( superoxides, hydrogen peroxide & hydroxyl ions)( superoxides, hydrogen peroxide & hydroxyl ions)

15. RECRUITMENT OF LEUCOCYTESRECRUITMENT OF LEUCOCYTES
TO SITE OF INJURYTO SITE OF INJURY
 INITIAL 6-24 HOURS– NEUTROPHILSINITIAL 6-24 HOURS– NEUTROPHILS
 LATER– MONOCYTES & LYMPHOCYTESLATER– MONOCYTES & LYMPHOCYTES
 Initially, it is the neutrophils that emigrate in the greatestInitially, it is the neutrophils that emigrate in the greatest
number, whereas lymphocytes, macrophages andnumber, whereas lymphocytes, macrophages and
eosinophils also take part in this process, initially ineosinophils also take part in this process, initially in
fewer numbers. As the inflammation regresses,fewer numbers. As the inflammation regresses,
decreasing numbers of neutrophils emigrate, whereasdecreasing numbers of neutrophils emigrate, whereas
more lymphocytes and macrophages make the trip andmore lymphocytes and macrophages make the trip and
finally predominate when the process becomes chronicfinally predominate when the process becomes chronic
with the disappearance of the neutrophils.with the disappearance of the neutrophils.

16. CELLULAR EVENTS
CHEMOTAXIS
 Definition:Definition: Process of directed cellProcess of directed cell
migration along a chemical gradientmigration along a chemical gradient
OrOr
 Movement of leukocytes along theMovement of leukocytes along the
chemical gradient.chemical gradient.
 It is responsible for the movement ofIt is responsible for the movement of
leukocytes towards the site of injuryleukocytes towards the site of injury

17. CHEMOTACTIC-AGENTS
 EXOGENOUSEXOGENOUS (from bacteria)(from bacteria)
BACTERIAL PRODUCTS-COMMONESTBACTERIAL PRODUCTS-COMMONEST
PEPTIDES OR LIPIDSPEPTIDES OR LIPIDS
 ENDOGENOUSENDOGENOUS ( from cells and plasma)( from cells and plasma)
COMPLEMENT COMPONENTS-C5aCOMPLEMENT COMPONENTS-C5a
LEUKOTRIENE B4LEUKOTRIENE B4
CYTOKINES-IL-8CYTOKINES-IL-8

18. PhagocytosisPhagocytosis
 DefinitionDefinition::
Engulfment ofEngulfment of
particulate matter orparticulate matter or
bacteria by the WBCsbacteria by the WBCs..

19. Stages of PhagocytosisStages of Phagocytosis
1. Chemotaxis1. Chemotaxis: Phagocytes are chemically: Phagocytes are chemically
attracted to site of infection ( C5a).attracted to site of infection ( C5a).
2. Recognition & Adherence:2. Recognition & Adherence: PhagocytePhagocyte
plasma membrane attaches to surface ofplasma membrane attaches to surface of
pathogen or foreign material.pathogen or foreign material.
 Adherence can be inhibited by capsules (Adherence can be inhibited by capsules (S.S.
pneumoniaepneumoniae) or M protein () or M protein (S. pyogenesS. pyogenes).).
 OpsonizationOpsonization: Coating process with opsonins: Coating process with opsonins
that facilitates attachment.that facilitates attachment. OpsoninsOpsonins includeinclude
antibodies (IgG) and complement proteinsantibodies (IgG) and complement proteins
(C3b).(C3b).

20. Stages of PhagocytosisStages of Phagocytosis
3. Ingestion3. Ingestion: Plasma membrane of: Plasma membrane of
phagocytes extends projectionsphagocytes extends projections
(pseudopods) which engulf the microbe.(pseudopods) which engulf the microbe.
Microbe is enclosed in a sac calledMicrobe is enclosed in a sac called
phagosomephagosome..
4. Digestion4. Digestion: Inside the cell, phagosome: Inside the cell, phagosome
fuses with lysosome to form afuses with lysosome to form a
phagolysosomephagolysosome..
Lysosomal enzymes kill most bacteriaLysosomal enzymes kill most bacteria
within 30 minutes and include:within 30 minutes and include:
Lysozyme: Destroys cell wall peptidoglycanLysozyme: Destroys cell wall peptidoglycan


21. Process of killingProcess of killing
 Oxygen dependentOxygen dependent
 Myeloperoxidase-Myeloperoxidase-
Halide systemHalide system
 Free radicalsFree radicals
 SuperoxidesSuperoxides
 Hydroxyl ionsHydroxyl ions
 Oxygen independentOxygen independent
 Lysosomal EnzymesLysosomal Enzymes
 Cat ionic proteinsCat ionic proteins

22. OUTCOMEOUTCOME
1. COMPLETE RESOLUTION1. COMPLETE RESOLUTION
RESTORATION OF SITE TO NORMALRESTORATION OF SITE TO NORMAL
LIMITED AND SHORT LIVED INJURYLIMITED AND SHORT LIVED INJURY
MINIMAL TISSUE DAMAGEMINIMAL TISSUE DAMAGE
REGENERATION OF PARENCHYMAL CELLSREGENERATION OF PARENCHYMAL CELLS
MACROPHAGES PLAYS AN IMPORTENT ROLEMACROPHAGES PLAYS AN IMPORTENT ROLE

23. OUTCOMEOUTCOME
2. FIBROSIS2. FIBROSIS
 EXTENSIVE TISSUE DAMAGEEXTENSIVE TISSUE DAMAGE
 TISSUES INCAPABLE OF REGENERATIONTISSUES INCAPABLE OF REGENERATION
 ABUNDANT FIBRIN-Eg SEROUS CAVITY-ABUNDANT FIBRIN-Eg SEROUS CAVITY-
GROWTH OF FIBROUS TISSUE LEADS TOGROWTH OF FIBROUS TISSUE LEADS TO
ORGANIZATIONORGANIZATION
3. PROGRESSION TO CHRONIC3. PROGRESSION TO CHRONIC
INFLAMMATIONINFLAMMATION

24. MORPHOLOGICAL PATTERNSMORPHOLOGICAL PATTERNS
OF ACUTE INFLAMMATIONOF ACUTE INFLAMMATION
Acute and chronic inflammation conformAcute and chronic inflammation conform
themselves into several appearances.themselves into several appearances.

25.  An effusion of thin fluidAn effusion of thin fluid
under acuteunder acute
inflammatoryinflammatory
conditions from aconditions from a
surface (oftensurface (often
mesothelial) is calledmesothelial) is called
serous inflammation.serous inflammation.
Eg. Blisters of skinEg. Blisters of skin
Bullous pemphigoidBullous pemphigoid
Dermis
SEROUSSEROUS InflammationInflammation
Blister fluid
Serous Exudate

26. Fibrinous Exudate
FIBRINOUSFIBRINOUS InflammationInflammation
•Fibrinous inflammation
consists of neutrophils admixed
with fibrin (e.g., fibrinous
pericarditis).
•The fibrin in this fluid can form
a fibrinous exudate on the
surfaces.
•Bread & Butter appearance
Here, the pericardial cavity has
been opened to reveal a
fibrinous pericarditis with
strands of stringy pale fibrin
between visceral and parietal
pericardium

27. CatarrhalCatarrhal inflammationinflammation
 Mucosa-lined surfaces may exhibitMucosa-lined surfaces may exhibit
catarrhal inflammationcatarrhal inflammation with thewith the
outpouring ofoutpouring of watery mucuswatery mucus..
 Eg. Common coldEg. Common cold

28. SuppurativeSuppurative InflammationInflammation
 SuppurativeSuppurative
inflammation (Purulent)inflammation (Purulent)
exudes pus, a mixture ofexudes pus, a mixture of
neutrophils and necroticneutrophils and necrotic
debris.eg.pyogenicdebris.eg.pyogenic
bacterial infection.bacterial infection.
Exuded yellowish fluid fluid in this
opened pericardial cavity also
contains a large number of acute
inflammatory cells. So it is a purulent
exudate

29. SUPPURATIVE INFLAMMATIONSUPPURATIVE INFLAMMATION
A A purulent exudate is seen beneath the meninges in theA purulent exudate is seen beneath the meninges in the
brain of this patient with acute meningitis frombrain of this patient with acute meningitis from
Streptococcus pneumoniae infection. The exudateStreptococcus pneumoniae infection. The exudate
obscures the sulci.obscures the sulci.
B The abdominal cavity is opened at autopsy here to revealThe abdominal cavity is opened at autopsy here to reveal
an extensive purulent peritonitis that resulted from rupturean extensive purulent peritonitis that resulted from rupture
of the colon.of the colon.
A B

30. ABSCESSABSCESS
 A localised (enclosed)A localised (enclosed)
collection of pus is calledcollection of pus is called
anan abscess.abscess.
 Extensive acuteExtensive acute
inflammation may lead toinflammation may lead to
abscess formation, asabscess formation, as
seen here with roundedseen here with rounded
abscesses (the purulentabscesses (the purulent
material has drained outmaterial has drained out
after sectioning to leave aafter sectioning to leave a
cavity) in the lungcavity) in the lung..

31.  Diverticulitis of ColonDiverticulitis of Colon
with abscesswith abscess
formationformation
AbscessAbscess
ABSCESSABSCESS
Sulfur granules ofSulfur granules of
actinomycosesactinomycoses
Lots of neutrophilsLots of neutrophils

32. ULCERULCER
 UlcerUlcer is a focal defect usually onis a focal defect usually on
an epithelial surface where thean epithelial surface where the
epithelium is entirely lacking;epithelium is entirely lacking;
 the exposed tissue is covered bythe exposed tissue is covered by
a fibrinopurulent exudatea fibrinopurulent exudate
(mixture of fibrin and(mixture of fibrin and
neutrophils).neutrophils).
 Eg. Peptic ulcer, Ophthus ulcerEg. Peptic ulcer, Ophthus ulcer

33. CellulitisCellulitis
cellulitiscellulitis denotes adenotes a
spreading acutespreading acute
inflammationinflammation
through interstitialthrough interstitial
tissuestissues